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Is Cancer a Metabolic Disease? The Answer of Metabolomics Volume...
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Is Cancer a Metabolic Disease? The Answer of Metabolomics Volume 2

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Advances in Metabolomics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 9617

Special Issue Editors

Dr. Daniel Oscar Cicero

E-Mail Website
Guest Editor
Department of Chemical Science and Technology, Università degli Studi di Roma Tor Vergata, 1, 00133 Rome, Italy
Interests: nuclear magnetic resonance; metabolomics; bladder cancer; cardiovascular diseases; metabolism and exercise
Special Issues, Collections and Topics in MDPI journals
Dr. Greta Petrella

E-Mail Website
Guest Editor
Department of Chemical Sciences and Technologies, Università degli Studi di Roma Tor Vergata, 1, 00133 Rome, Italy
Interests: metabolomics; NMR; cellular metabolism; cancer; urinary biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is almost unanimously considered to be the result of genetic alterations at the nuclear level of oncogenes and tumor-suppressor genes. This theory is considered almost a dogma, to the point that the National Cancer Institute states that “Cancer is a genetic disease—that is, it is caused by changes to genes that control the way our cells function, especially how they grow and divide”. In this context, the metabolic changes observed in cells, tissues, and organisms are the consequence of these genetic signatures. However, several inconsistencies of this theory have been observed, giving rise to an alternative explanation of cancer as a disease that begins with a mitochondrial metabolic dysfunction, in some sense returning to Otto Warburg’s original observation. Recent data indicate, however, that mitochondrial metabolism can be down- or upregulated, giving rise to two types of tumors: oxidative and nonoxidative. From this perspective, metabolic alterations are the cause of the genetic alterations that influence the development of cancer. What causes metabolic alteration is a matter of discussion, but potential candidates are increased inflammation, increased ROS formation, and overstimulation of PARPs. Although we do not yet have enough evidence to fully embrace the metabolic theory, or to accurately weight the relative importance that both factors—genetic mutations and metabolic alterations—play in the origin of the disease, metabolomics can make a significant contribution. The fact that metabolism can have a crucial role places it on the same level as genomics and transcriptomics for the diagnosis and prognosis of cancer, and assigns it a unique place for the discovery of new specific therapeutic targets. In this exciting field, we still have almost everything to discover and much to gain in the understanding of a disease that has become one of the most demanding challenges of modern medicine.

Dr. Daniel Oscar Cicero
Dr. Greta Petrella
Guest Editors

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Keywords

  • cancer metabolism
  • metabolomics
  • carcinogenesis
  • cancer biomarkers

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Published Papers (3 papers)

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Research

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13 pages, 2587 KiB  
Article
Metabolomic Signatures in Doxorubicin-Induced Metabolites Characterization, Metabolic Inhibition, and Signaling Pathway Mechanisms in Colon Cancer HCT116 Cells
by Raja Ganesan, Vasantha-Srinivasan Prabhakaran and Abilash Valsala Gopalakrishnan
Metabolites 2022, 12(11), 1047; https://doi.org/10.3390/metabo12111047 - 31 Oct 2022
Cited by 5 | Viewed by 2389
Abstract
Doxorubicin (DOX) is a chemotherapeutic agent is used for various cancer cells. To characterize the chemical structural components and metabolic inhibition, we applied a DOX to HCT116 colon cancer cells using an independent metabolites profiling approach. Chemical metabolomics has been involved in the [...] Read more.
Doxorubicin (DOX) is a chemotherapeutic agent is used for various cancer cells. To characterize the chemical structural components and metabolic inhibition, we applied a DOX to HCT116 colon cancer cells using an independent metabolites profiling approach. Chemical metabolomics has been involved in the new drug delivery systems. Metabolomics profiling of DOX-applied HCT116 colon cancer cellular metabolisms is rare. We used 1H nuclear magnetic resonance (NMR) spectroscopy in this study to clarify how DOX exposure affected HCT116 colon cancer cells. Metabolomics profiling in HCT116 cells detects 50 metabolites. Tracking metabolites can reveal pathway activities. HCT116 colon cancer cells were evenly treated with different concentrations of DOX for 24 h. The endogenous metabolites were identified by comparison with healthy cells. We found that acetate, glucose, glutamate, glutamine, sn-glycero-3-phosphocholine, valine, methionine, and isoleucine were increased. Metabolic expression of alanine, choline, fumarate, taurine, o-phosphocholine, inosine, lysine, and phenylalanine was decreased in HCT116 cancer cells. The metabolic phenotypic expression is markedly altered during a high dose of DOX. It is the first time that there is a metabolite pool and phenotypic expression in colon cancer cells. Targeting the DOX-metabolite axis may be a novel strategy for improving the curative effect of DOX-based therapy for colon cancer cells. These methods facilitate the routine metabolomic analysis of cancer cells. Full article
(This article belongs to the Special Issue Is Cancer a Metabolic Disease? The Answer of Metabolomics Volume 2)
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Review

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27 pages, 2238 KiB  
Review
The Role of Reprogrammed Glucose Metabolism in Cancer
by Meran Keshawa Ediriweera and Sharmila Jayasena
Metabolites 2023, 13(3), 345; https://doi.org/10.3390/metabo13030345 - 25 Feb 2023
Cited by 15 | Viewed by 4502
Abstract
Cancer cells reprogram their metabolism to meet biosynthetic needs and to adapt to various microenvironments. Accelerated glycolysis offers proliferative benefits for malignant cells by generating glycolytic products that move into branched pathways to synthesize proteins, fatty acids, nucleotides, and lipids. Notably, reprogrammed glucose [...] Read more.
Cancer cells reprogram their metabolism to meet biosynthetic needs and to adapt to various microenvironments. Accelerated glycolysis offers proliferative benefits for malignant cells by generating glycolytic products that move into branched pathways to synthesize proteins, fatty acids, nucleotides, and lipids. Notably, reprogrammed glucose metabolism and its associated events support the hallmark features of cancer such as sustained cell proliferation, hijacked apoptosis, invasion, metastasis, and angiogenesis. Overproduced enzymes involved in the committed steps of glycolysis (hexokinase, phosphofructokinase-1, and pyruvate kinase) are promising pharmacological targets for cancer therapeutics. In this review, we summarize the role of reprogrammed glucose metabolism in cancer cells and how it can be manipulated for anti-cancer strategies. Full article
(This article belongs to the Special Issue Is Cancer a Metabolic Disease? The Answer of Metabolomics Volume 2)
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Other

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6 pages, 745 KiB  
Perspective
Cancer Cachexia and Dysregulated Phosphate Metabolism: Insights from Mutant p53 and Mutant Klotho Mouse Models
by Ronald B. Brown
Metabolites 2022, 12(12), 1284; https://doi.org/10.3390/metabo12121284 - 17 Dec 2022
Cited by 6 | Viewed by 1897
Abstract
The present perspective article proposes that cachexia, muscle wasting in cancer, is mediated by dysregulated phosphate metabolism and phosphate toxicity that can damage tissues in most major organ systems. A diet high in phosphorus fed to mice deficient in klotho, a cofactor that [...] Read more.
The present perspective article proposes that cachexia, muscle wasting in cancer, is mediated by dysregulated phosphate metabolism and phosphate toxicity that can damage tissues in most major organ systems. A diet high in phosphorus fed to mice deficient in klotho, a cofactor that regulates phosphate metabolism, accelerates aging, sarcopenia, general organ atrophy, kyphosis, and osteoporosis. Similar effects are seen in phenotypes of mutant p53 mice that overexpress the p53 tumor suppressor gene. Although mutant p53 mice do not develop tumors compared to wild-type mice, mutant p53 mice have shorter mean lifespans. Furthermore, tumorigenesis is associated with the sequestration of excessive inorganic phosphate, and dangerous levels of phosphate are released into circulation during tumor lysis syndrome. In total, this evidence implies that tumorigenesis may be a compensatory mechanism that provides protective effects against systemic exposure to dysregulated phosphate metabolism and phosphate toxicity related to cachexia in cancer. Moreover, the hypothetical protection against phosphate toxicity afforded by tumorigenesis also provides an alternate explanation for putative tumor evasion of the immune system. Insights proposed in this perspective paper provide new directions for further research, with potential to develop novel interventions and clinical applications that modify dietary phosphate intake to reduce cachexia in cancer patients. Full article
(This article belongs to the Special Issue Is Cancer a Metabolic Disease? The Answer of Metabolomics Volume 2)
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